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Definition
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| What is the common name for the orthomyxoviruses? |
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Definition
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Term
| What structure do orthomyxoviruses have? |
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Definition
| These viruses have an enveloped nucleocapsid with two kinds of spike proteins (hemagglutinin and neuraminidase) protruding on the virus surface. The virion packs its RNA-dependent RNA polymerase with the nucleocapsid. |
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| What are the two spike proteins of the orthomyxoviruses? |
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Definition
| hemagglutinin and neuraminidase which protrude on the virus surface. |
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Term
| Whose RNA polymerase does the orthomyxoviruse use? |
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Definition
| Viral RNA dependent RNA polymerase |
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Term
| How do orthomyxoviruses infect the cell? |
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Definition
| The virion packs its RNA-dependent RNA polymerase with the nucleocapsid. Hemagglutinin binds to its receptor sialic acid on the host cell surface, where the virus is endocytosed. The viral envelope fuses with the endosomal membrane to release the -strand RNAs (8 of them, all different) and viral proteins into the cytoplasm. These RNAs and proteins move into the nucleus, where the viral RNA-dependent RNA polymerase synthesizes mRNAs from the -strand templates. |
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| How do orthomyxoviruses infect the cell?(part 2) |
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Definition
| The polymerase also makes +strand RNA (called complementary RNA, or cRNA), and uses this +strand RNA as the template to make more –strand RNA. The mRNAs move into the cytoplasm, and are translated by the host to make capsid proteins, hemagglutinin and neuraminidase. The hemagglutinin and neuraminidase are exported to the cell plasma membrane. The nucleocapsid proteins are transported into the nucleus, and assemble with the viral. strand RNA to make the nucleocapsid. This nucleocapsid leaves the nucleus and moves to the plasma membrane, where it ( 8 of them, which contains 8 different -strand viral RNAs) assembles with many copies of the two spike proteins, and buds from the plasma membrane. |
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Term
| How do orthomyxoviruses leave the cell? |
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Definition
| The neuraminidase cuts the sialic acid so that the virions are freed from the cell surface. |
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Term
| How do anti-flu drugs work? |
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Definition
The anti-flu drugs zanamivir and oseltamivir (also called tamiflu) bind to neuraminidase and block its activity, reducing the release of progeny virions.
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| Why do new influenza vaccines need to be created this year? |
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Definition
| Influenza and other RNA viruses mutate very rapidly, and the structure of the spikes can vary greatly from year to year (a form of evolution-the fittest viruses; those most able to evade our immune system-survive). As a result, a new influenza vaccine must be administered each year. |
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| The Spanish flue killed more or less people then Aids combined? Where do epidemics often begin? |
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Definition
Flu epidemics killed more people in a single year (Spanish flu in 1918) than has all AIDS deaths combined! That epidemic may have started in Fort Riley (previously Fort Funston), KS! Epidemics today often begin in regions where humans, pigs, and chickens live in crowded close quarters. |
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Definition
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| What are some negative stranded RNA viruese? |
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Definition
-orthomyxoviruse
-Filoviruses
-Lyssaviruses
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Definition
Filoviruses are filamentous viruses with a membrane envelope. They include the viruses such as Ebola virus that causes hemorrhagic fever.
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Definition
Lyssaviruses, which includes Rabies virus, are bullet-shaped, and are enveloped viruses.
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| What is the difference between the Influenza virus and the Filovirus and Lyssaviruses? |
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Definition
| Unlike influenza virus, Filoviruses and Lyssaviruses assemble in cytoplasm, without using the nucleus. |
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Term
| What is the structure of the HIV virus? What does it have in its virion? |
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Definition
| Its +strand RNA genome is encased by a cone-like capsid, surrounded by an envelope that contains protein spikes. In addition to two molecules of +strand RNA, HIV also packages two tRNA molecules, two molecules of integrase, and two molecules of reverse transcriptase (this is an RNA-dependent DNA polymerase). |
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Term
| What receptor does HIV bind to on the host Tcell? |
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Definition
| HIV binds to CD4 as its receptor on the host Tcell. |
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| How does the HIV virus infect the T cell? |
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Definition
| HIV binds to CD4 as its receptor on the host Tcell. When infecting a cell, the viral envelope fuses with the host cell plasma membrane to release the capsid into the cytoplasm. Reverse transcriptase makes DNA from the RNA (using the tRNAs as primers). This enzyme also carries the ribonuclease H activity which degrades the RNA. Reverse transcriptase then makes dsDNA from the remaining -strand DNA. This dsDNA then moves into the nucleus, and integrates itself into the host cell chromosome to form a provirus. This integration is catalyzed by another viral enzyme called integrase. |
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Definition
The provirus is transcribed to make mRNA and to provide more +strand RNA for packaging. The mRNA moves into the cytoplasm, is translated by the host ribosome to make proteins. All retroviruses encode a Gag protein (making the capsid proteins), Pol (=reverse transcriptase + integrase + HIV protease), and Env (=envelope spikes=gp120 + gp41). The HIV protease then cleaves these polypeptides into individual proteins. Viral proteins and RNA assemble at the plasma membrane, and finally the capsid buds out of the cell surface, acquiring an envelope from the plasma membrane.
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| Whose ribosome does the HIV virus use? |
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Definition
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Definition
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| What have drug been targeting as far as combating the HIV infection? |
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Definition
| We mentioned that the reverse transcriptase, the integrase and the protease have been targets for drug development because of their critical roles in HIV lifecycle. However, like all RNA viruses, HIV has a high mutation rate. These drugs are often used in combination, to try to prevent formation of a virus resistant to one drug (it's much less likely to develop two mutations simultaneously than a single resistance mutation) |
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Term
What is a mutualistic relationship?
What is a commensal relationship? |
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Definition
Many creatures live in symbiotic relationship with one another.
-A mutualistic relationship benefits both creatures.
-A commensal relationship benefits one creature and neither helps nor hurts the other.
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Term
| What is a parasitic relationship? |
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Definition
- A parasitic relationship benefits one creature at the expense of the other. Most species are parasitic. Viruses are by definition parasites, as are all microbes that cause human diseases.
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Term
| What parasite causes 300 million cases and 1 million deaths a year? What is it cause by? |
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Definition
We looked at a parasite of great medical importance: Malaria (300 million cases of infection and ~1 million death annually)
-It is caused by the protozoan Plasmodium. Plasmodium falciparum and Plasmodium vivax account for most of Malaria cases.
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| What is the life cylce of the Plasmodium? |
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Definition
Protozoan sporozoites (haploid-1n, 1 copy of all its chromosomes) are transmitted from mosquito Anopheles saliva into our blood system, where they change into merozoites (still haploid-1n) that invade our liver. The parasite multiplies there via mitosis and within red blood cells, dividing every 72 hours, and lysing blood cells. Eventually, some of the merozoites develop into gametocytes (still haploid-1n) that remain within red blood cells, and are picked up by the mosquito. |
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| What is the life cylce of the Plasmodium?(part 2) |
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Definition
| In the mosquito gut, the red blood cells are lysed to release the gametocytes, which then undergo fertilization in the mosquito gut to form ookinetes (diploid-2n, 2 copies of all chromosomes). The ookinetes migrate out of the gut, form oocysts, and eventually form new haploid (1n) sporozoites via meiosis (also termed sporogony). These new sporozoites move to the salivary gland. |
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| When does the Plasmodium become diploid? |
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Definition
| In the mosquito gut it undergoes fertilization forming ookinetes (diploid-2n, 2 copies of all chromosomes) |
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Term
There is an exogenous asexual phase in the mosquito called sporogony during which the parasite multiplies. There is also an endogenous asexual phase that takes place in the vertebrate or human host that is called schizogony. This phase includes the parasite development that takes place in the red blood cell, called the erythrocytic cycle and the phase that takes place in the parenchymal cells in the liver, called the exo-erythrocytic phase. |
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Definition
| The exo-erythrocytic phase is also called the tissue phase. The schizogony that takes place here can occur without delay during the primary infection or can be delayed in the case of relapses of malaria. I will focus on the development of the parasite in the human host. |
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Definition
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| What are the general barriers that prevent infections? |
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Definition
-being healthy -good nutrition -age-babies and elderly are most susceptible
-fever-higher body temperature kills some bacteria and slows some viral replication. Some bacterial components, especially lipopolysaccharide, induce fever.
-genetic factors-mutation of hemoglobin in sickle-cell anemia patients; usually unknown aspects of a person’s genetic background make some people more or less susceptible to a particular disease.
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Term
| What are physical barriers that prevent viruses from getting into the body? |
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Definition
-Skin-a dry surface
-Washing removes microbes
-Dead skin sloughs off regularly
-Mucosa on internal surfaces exposed to bacteria-the intestines, lungs, reproductive tracts
-Urination removes bacteria from the urethra
-Length of urethra slows bladder infection.
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| What are chemical barriers to an infection? |
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Definition
-Oil on the skin
-Soap kills many bacteria
-Lysozyme secreted by eyes dissolves peptidoglycan
-Stomach acid, liver bile, pancreatic and intestinal enzymes kill bacteria
-Acid secreted by bacteria in the female reproductive tract kills bacteria. Neutralization of this acid can cause infections.
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| What are some biological barriers to infections?(activly kill the bacteria) |
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Definition
-Immobile phagocytes of the reticuloendothelial system phagocytose bacteria.
-Indigenous microbes in the intestine and reproductive tracts, and on the skin, kill other bacteria by secreting bacteriocins, eating any available food, and taking up places to which parasites could attach.
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Term
| When a tissue is damaged, what alarm signal is created by neighboring cells? What is one of our bodies most complicated responses to infection? |
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Definition
| One of the most complicated biological barriers is our body's general response to localized infection, inflammation. When tissue is damaged, burst dead cells cause neighboring cells to produce an alarm signal, bradykinin. |
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Term
| How does inflamation work? |
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Definition
| Bradykinin binds to mast cells near capillaries (and also basophils in tissues), and causes them to degranulate to release large amounts of histamine. Histamine in turn binds to capillary cells and causes them to change shape slightly and widen cell-cell junctions (vasodilation), to permit liquid from the blood stream to enter the tissue. This causes the localized swelling of inflammation, as well as localized reddening, since some red blood cells leak into the tissue, along with platelets and clotting factors that help seal off the area, preventing any invaders from spreading to other areas. |
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| How does inflamation work?(part 3) |
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Definition
They are aided in phagocytosing bacteria by the presence of C3b receptors on the neutrophil surface. Bacterial LPS binds to the complement protein C3b secreted by our bodies, leading to coating of invading bacteria by complement C3b. This is called opsonization, and it helps neutrophils to bind to and engulf bacteria. Several complement proteins can work together to form a membrane attack complex, which drills a pore in bacterial plasma membrane and eventually kill the bacterium. |
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| What is an example of non-specific(innate) immunity? |
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Definition
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| What are some examples of specific immunity(adaptive)? |
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Definition
T and B Cells
Clonal Deletion
Generation of Diversity
Cellular Immunity
Antibodies
Humoral Immunity
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Term
| Epithelia in the human airway? |
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Definition
In human airway epithelia, these motile cilia bear receptors that detect bitter compounds and signal the cilia to increase their rhythmic beat frequency to help clear noxious substances from the lungs. |
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| Where are the 4 types of adaptive immune system cells born? What do they do? |
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Definition
| The specific or adaptive immune system consists primarily of 4 types of cells: Helper T cells (TH cells), cytotoxic T cells (TC cells), B cells, and Macrophages. These cells are born in the bone marrow, but mature in various other places. They recognize antigens: proteins or pieces of proteins (or nucleic acids or carbohydrates) that can be bound by receptor proteins on the surfaces of the T and B cells |
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How do Tcells work? How do they decide what antigen they bind to?
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Definition
| Each T Cell is covered with hundreds of identical T Cell Receptors, each of which is capable of binding a single antigen. Any two T Cells will bind to two different antigens, however, because their T cell Receptors are different. Upon birth, the antigen to which the T Cell will bind is randomly established. The T cells travel to the thymus gland, where they are presented with essentially all the antigens normally present in the human body. |
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How do Tcells work? How do they decide what antigen they bind to?(part 2)
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Definition
| If the immature T Cell can bind to an antigen at this point, it undergoes apoptosis (programmed cell death) and dies; this is called clonal deletion. 95% of all immature T cells die, leaving ONLY those T cells that can bind to antigens not normally found in the human body, i.e. foreign antigens. |
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| What happens if a T-Cell that binds to an antigen that is present in the body normally surivives? |
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Definition
| If a T-Cell survives that reacts to an antigen that is normally present in our body, it can cause an autoimmune disease, such as rheumatoid arthritis, systemic lupus, etc. |
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| What do our cells normally do to Tcells? |
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Definition
Our cells normally present their antigens to T cells all the time. As proteins are turned over in our cells, they cut up their proteins and other components and place the bits in the MHC (Major Histocompatibility Complex) Class I molecule on the cell surface. The T cell recognizes the MHC Class I molecule, and looks in it to see what antigen is presented. If a mature T Cell can bind to that antigen, the T cell reacts to set off an immune response.
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| What is the mechanism in which our immune system creates diverse T cell receptors? |
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Definition
The mechanism by which our immune system generates so many diverse T-Cell Receptors is unique, and is explained by looking at the structure of the T Cell Receptors, and the genes encoding these proteins. The genes there include a variety of exons (regions of the gene that actually are used to encode proteins), that are brought together through splicing of DNA to make a random combination of antigen-binding regions.
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Term
| What are two types of protesin that compose T cell receptors? |
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Definition
| Each T-Cell Receptor (TCR) is composed of two types of proteins, an alpha (light) chain, and a beta (heavy) chain. The beta chain has a variable region, a diversity region, a joint region and a constant region (V-D-J-C). The alpha chain has a variable region, a joint region and a constant region (V-J-C). |
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| Where is the Tcell receptor? What bond links the proteins? |
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Definition
The T-Cell receptor is always membrane-bound and each T-Cell Receptor has one copy of each of these proteins (the alpha and beta chains). Both of these proteins are embedded in the plasma membrane of the T Cell, and are linked to each other by a disulfide bond. The constant region has the same amino acid sequence in all T Cells. |
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Term
How do Tcell receptors generate diversity among receptors?
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Definition
The variable region is different, however, in every T Cell. There is not enough coding capacity in the human genome to encode all of the billion possibilities of T Cell receptors, so the T Cells use some genetic tricks to generate this great diversity of receptors. The variable regions of the T Cell Receptor are encoded in consecutive pieces (exons) along the length of DNA. Upon T Cell birth, these pieces are brought together in an orderly, but random manner, to create a single T-Cell Receptor alpha chain gene, and a single T-Cell Receptor beta chain gene. |
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| How do Tcell receptors generate diversity among receptors?(part 2) |
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Definition
| The mechanism of bringing these pieces together is by splicing the DNA together permanently; that is, to excise the DNA between the chosen pieces. The alpha chain splices a V and J region together, the beta chain splices a V, D, and J region. After transcription, the RNA containing the newly formed VJ or VDJ variable regions are spliced to the single constant region to form a mature mRNA that can be translated to make a protein with a VDJ region unique to that cell connected to a constant region found in all T-Cell Receptors. |
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Term
| How do orthomyxoviruses infect the cell?(part 3) |
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Definition
| -strand RNA to make the nucleocapsid. This nucleocapsid leaves the nucleus and moves to the plasma membrane, where it (actually 8 of them, which contains 8 different -strand viral RNAs) assembles with many copies of the two spike proteins, and buds from the plasma membrane. |
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